Central Causation of Autism/ASDs via Excessive [Ca2+]i Impacting Six Mechanisms Controlling Synaptogenesis during the Perinatal Period: The Role of Electromagnetic Fields and Chemicals and the NO/ONOO(-) Cycle, as Well as Specific Mutations

Overview

This study explores the central causative roles of excessive intracellular calcium ([Ca2+]i) during perinatal development in the pathogenesis of autism spectrum disorders (ASDs). While the topics of perinatal development, [Ca2+]i, and disrupted synaptogenesis have been previously discussed in the context of ASD, this paper introduces a novel focus on six specific mechanisms of synaptogenesis, all regulated by [Ca2+]i, and commonly found to be abnormal in ASDs.

Findings

• Autism epidemic causation centrally involves exposure to both electromagnetic fields (EMFs) and various chemicals.
• EMFs raise [Ca2+]i through the activation of voltage-gated calcium channels (VGCCs).
• Fifteen classes of chemicals implicated in autism each elevate [Ca2+]i—twelve through NMDA receptor activation and three through distinct mechanisms.
• The chronic nature of ASD can be explained by the persistent activation of the NO/ONOO(-) vicious cycle and MeCP2-related epigenetic dysfunction.
• Many cases of genetic causation also involve mechanisms that increase [Ca2+]i or otherwise impact synaptogenesis.
• The literature review supports each of these mechanistic steps as predicted by the presented model.

Conclusion

The paper discusses strategies to prevent or treat ASDs, emphasizing the avoidance of EMF and chemical exposure, as well as the use of nutrients (such as those raising Nrf2 levels), enriched environments, vitamin D, magnesium, and omega-3s to offer potential benefits. This model underscores the significant connection between EMF exposure and health risks related to ASD.